Cessation of breathing during sleep for more than 10 seconds is called an “apnea,” which leads to decreased blood oxygenation and disruption of sleep. Apneas are traditionally categorized as central, where there is no respiratory effort, or obstructive sleep apnea (OSA), where there is respiratory effort but the airway is blocked. With purely central apneas, the airway is patent (or open), but the patient is not attempting to breathe. With other central apneas and all obstructive apneas, the airway is not patent (i.e., it is occluded). The occlusion is usually at the level of the tongue or soft palate.
The common form of treatment of apneas is the administering of continuous or variable positive airway pressure (referred to herein generally as CPAP). Devices that provide CPAP treatment are described in U.S. Pat. Nos. 5,704,345, 6,532,957, 6,575,163, 6,484,719, 6,688,307, and 6,532,959, incorporated herein by reference. The procedure for administering CPAP treatment has been well documented in both the technical and patent literature. Briefly stated, CPAP treatment acts as a pneumatic splint of the airway by the provision of positive pressure, usually in the range 4-20 cm H2O. The air is supplied to the airway by a motor driven blower whose outlet passes air via a delivery tube or hose to a nose (and/or mouth) mask sealingly engaged to a patient's face. An exhaust port is provided in the delivery tube proximate to the mask.
More sophisticated forms of CPAP, such as bi-level CPAP and self-titrating CPAP, are described in U.S. Pat. Nos. 5,148,802 and 5,245,995, respectively.
CPAP therapy is also known to be beneficial to some cardiac pathology, for example, congestive heart failure. By boosting intrathoracic pressure, CPAP offers various (potential) direct benefits in heart failure, for example, impeding venous return (reducing preload), reducing the systolic pressure gradient against which the left ventricle must pump (reduced afterload), and reducing left-ventricular trans-mural pressure (improved contractile efficiency). In addition, CPAP may offer indirect benefits to heart-failure patients, e.g., to counter pulmonary edema, to increase lung volume (may aid ventilatory stability in Cheyne-Stokes respiration), and in patients with a disposition to obstructive apnea, to reduce sympathetic activation through prevention of repetitive OSA.
Various techniques are known for detecting abnormal breathing patterns indicative of obstructed breathing. U.S. Pat. No. 5,245,995, for example, describes how snoring and abnormal breathing patterns can be detected by inspiration and expiration pressure measurements while sleeping, thereby leading to early indication of pre-obstructive episodes or other forms of breathing disorder. Patterns of respiratory parameters are monitored, and CPAP pressure is raised on the detection of pre-defined patterns to provide increased airway pressure to subvert the occurrence of the obstructive episodes and the other forms of breathing disorder.
Central apneas need not involve an obstruction of the airway, and often occur during very light sleep and in patients with various cardiac, cerebrovascular and endocrine conditions unrelated to the state of the upper airway. In cases where the apnea is occurring without obstruction of the airway, there may be little benefit in increasing CPAP pressure, in contrast to an obstructive apnea.
To differentiate between central and obstructed apneas, U.S. Pat. No. 6,029,665, incorporated herein by reference, teaches a CPAP system that monitors pulsatile airflow during the apnea event. With each beat of the heart, of the order of 66 ml of blood is ejected from the chest over about 0.3 sec, producing a pulsatile blood flow out of the chest of the order of 0.22 l/sec peak flow. If the chest wall were rigid this would create a partial vacuum in the chest cavity, and, if the upper airway were open and had zero flow resistance, a similar quantity of air would be sucked in through the trachea. In practice, the chest wall is not totally rigid, and the airways have finite airflow resistance. Consequently the measurable airflow (or cardiogenic oscillation) with each beat of the heart is of the order of 0.02 to 0.1 I/sec.
If there is a central apnea with an open airway, the device of the '665 patent will sense cardiogenic oscillations in the air pressure, and determine that an unobstructed central apnea event has occurred. Conversely, if the airway is closed, the pressure waveform will not have any noticeable cardiogenic oscillations, and the device of the '665 patent will determine that the apnea event was an obstructed event.
Implementing the apparatus and method of the '665 patent prevents the inappropriate increase in the splinting CPAP air pressure during a central apnea, thereby preventing an unnecessary increase in pressure that may otherwise reflexively inhibit breathing and further aggravate the breathing disorder. The device is also used in a diagnostic mode, using nasal cannulae in the place of a face mask, where measurements of apneas, patency, and partial obstruction are logged, but no CPAP treatment is effected. The data provides a physician with the ability to diagnose conditions such as OSA and upper airway resistance syndrome.
Neither the '665 patent nor other prior art utilizes measurements of cardiogenic oscillations in a CPAP patient's airflow for monitoring or treating conditions related to cardiac health.